Female Genital System

Vulva -more inflammatory than life threatening ds

Vulvitis -Pruritus
-5 most impt infxns:
-HPV – condylomata acuminate and vulvar intraepithelial
neoplasia
-HSV 1 or 2
-gonococcal suppurative infxn of vulvovaginal glands
-syphilis with primary chancre
-candidal vultitis
Non-neoplastic -atrophic thinning or hyperplastic thickening
Epithelial Ds -2 forms:
-1) lichen sclerosus
-2) lichen simplex chronicus
-can co-exist
-may look like leukoplakia (also see in vitiligo, benign dermatoses
like psoriasis and lichen planus, carcinoma in situ, Paget dx, and
invasive carcinoma)
1) Lichen Sclerosus -rete pegs
-thin epidermis
-superficial hyperkeratosis and dermal fibrosis
-white plaques, parchment-like
-labia atrophic, vaginal constriction
-m/c postmenopausal
-a/i?
2) Lichen Simplex -epithelial thickening w/ significant hyperkeratosis
Chronicus -looks like leukoplakia
-more mitotic activity and leukocyte infiltration
-epithlium no atypia
-at margins of cancer but does not increase risk of CA
Vulvar Tumours -1) condylomas and low-grade vulvar intraepithelial neoplasia (VIN I)
-2) high grade vulvar intraepithelial neoplasia (VIN II or III) and
carcinoma of the vulva
-3) extramammary Paget Disease
-4) melanoma of vulva
1) VIN I -condylomas – anogenital warts
-two categories
-1) condylomata lata (uncommon or in secondary syphilis – flat
moist lesions)
-2) condylomata acuminate – m/c (papillary and elevated or flat
and rugose)
-red to pink to brown
-HPV 6 and 11
-low malignant potential
2) VIN II or III or -m/c > 60yoa
carcinoma of vulva -90% squamous cell carcinomas
-2 biological forms:
-1) HPV – younger, smokers
-2) not HPV – older, preceded by non-neoplastic epithelial changes
(more lichen sclerosus)
 -less than 2cm, 75% survival after surgery
Vagina -seldom site of primary disease
-congenital anomalies uncommon
Vaginitis -leukorrhea
-usually Candida albicans and Trichomonas vaginalis
-C albicans – curdy white d/c
-T vaginalis – water gray-green d/c
Vaginal Intraepithelial -very uncommon
Neoplasia and Squamous -concurrence of neoplasms in other sites – probably viral
Cell Carcinoma -vaginal clear cell adenocarcinoma – teenage girls with mothers who
took Diethylstilbestrol during preg
Cervix -barrier
-usually banal inflammations (Cervicitis)
-squamous cell carcinoma
Cervicitis -inflammations extremely common
-mucopurulent to purulent vaginal d/c
-either non-infxs or infxs
-Chlamydia trachomatis, T. vaginalis, Candida, N gonorrhoeaea, HSV
II and HPV
-STD
-C trachomatis m/c by far
-dysplastic change can increase CA risk (HPV)
Tumours of Cervix -cervical carcinoma – CA related deaths
-endocervical polyp
Cervical Intraepithelial -incidence of precursor CIN has increased
Neoplasia and Squamous -squamous cell carcinoma arises from CIN
Cell Carcinoma -PAP test (pre CA can be seen as long as 20 yrs prior)
CIN -CIN I – mild dysplasia
-CIN II – moderate dysplasia
-CIN III – severe dysplasia and carcinoma in situ
-not always progress to CA
-risk factors: early 1st intercourse, multiple partners, male partner with
multiple previous partners, HPV infxn, other
-HPV 16 and 18
Invasive carcinoma of -m/c squamous cell carcinoma, from CIN
the cervix -rest are adenocarcinoma or adenosquamous carcinomas, small cell
neuroendocrine carcinomas
-1-3 grade on cellular differentiation and stage 1-4 on spread
Endocervical Polyp -m/b inflammatory
-soft, smooth glistening surface with dilated spaces with mucinous
secretion
-lesions on top may bleed, but no malignant potential
Body of Uterus -many disorders, common, chronic, recurrent
Endometritis -relatively resistant to infections
-acute rxns – bacterial after parturition or miscarriage
-chronic endometritis – follows chronic gonorrheal pelvic ds, TB,
endometrial cavities after preg, IUDs, idiopathic
Endometriosis -endometrial tissue in pelvis
-3 possibilities:
-1) regurgitation theory: menstrual backflow
 -2) metaplastic theory: endometrial or coelomic
-3) vascular or lymphatic dissemination theory: extrapelvic or
intranodal
Dysfunctional Uterine -abnormal bleeding in absences of well-defined organic lesion in
Bleeding uterus
-4 functional groups
-1) failure of ovulation: proliferative but no secretory
-2) inadequate luteal phase: corpus luteum problem with decreased
progesterone
-3) contraceptive-induced bleeding: usually BCP
-4) endomyometrial ds: chronic endometritis, polyps, submucosal
leiomyomas
Endometrial Hyperplasia -xs estrogen to progestin
-simple, complex, atypical
-may rise to carcinoma of endometrium
Tumours of -m/c polyps leiomymoas, carcinomas
Endometrium and -all get bleeding as earliest manifestation
Myometrium
Endometrial Polyps -hemispherical
-may project into uterine cavity
-usually at menopause
-abnormal uterine bleeding, may lead to CA
Leiomyoma and -fibroids – benign tumours from smooth muscle cells
Leiomyosarcoma -related to estrogen and BCP
-menorrhagia w/ or w/o metrorrhagia
-leiomyosarcoma – mesenchymal cells or myometrium
-usually solitary (unlike leiomyoma)
-recurrence common with removal
Endometrial Carcinoma -m/c CA of female genital tract
-55-65yoa
-risk: obesity (increase estrogen), DM, HTN, infertility
-usu late-metastasizing neoplasms
-increase estrogen is a risk
-some that aren’t associated with estrogen have poorer prog
Fallopian Tubes -seldom site of primary disease
-usually inflammation – PID
- ectopic pregnancy, endometriosis, rare primary tumours
-usually inflammation of the tubes with bacteria
-now usu – strep and staph
-nongonococcal now more invasive, bloodborne infections (HT, BR,
joints)
-salpingitis sxs: fever, lower pelvic pain, pelvic masses, obstruction of
tubal lumina
-primary adenocarcinomas – if start here, not usually found until
spread
Ovaries -infrequently primary site of disease except neoplasms
-CA of ovary more deaths
Follicle and Luteal Cysts -very common
-in unruptured graafian follicles or in follicles that rupture and
immediately sealed
 -multiple, under ovarian serosal covering
-small, filled with clear serous fluid
-rupture  intraperitoneal bleeding and acute abd sxs
Polycystic ovaries -oligomenorrhea, hirsutism, infertility, obesity
-secondary to excessive estrogens and androgens
-aka stein-leventhal syndrome
-big ovaries, gray-white smooth outer cortex, with subcortical cysts
-xs androgens, xs LH, low FSH
Tumours of Ovaries -3 cell types normally: multipotential surface (coelomic) covering
epithelium, totipotential germ cells, multipotential sex cells
-usually neoplasms of surface epithelial origin
-risk: nulliparity and family history
-BCP reduce risk
-BRCA genes often there
Surface epithelial- -from coelomic epithelium
stromal tumours -have intermediate borderline category – tumours of low malignant
potential
Serous Tumours -most frequent ovarian tumours
-aka cystadenomas or cystadenocarcinomas
-usually borderline and malignant lesions
Mucinous Tumours -epithelium has mucin-secreting cells like those in endocervical
mucosa
-less malignant
-cystadenocarcinomas – malignant, better prognosis
Endometrioid Tumours -solid or cystic
-mass projecting from wall of an endometriotic cyst filled with
chocolate-coloured fluid
-usually malignant
-b/l, 30% have concomitant endometrial carcinoma
Other Ovarian -teratomas of germ-cell origin
Tumours
Teratomas -neoplasms of germ-cell origin
-younger px = greater is likelihood of malignancy
-90% - benign cystic mature teratomas
1) Benign (mature) -dermoid cysts – cyst lined by recognizable epidermis replete with
cystic teratomas adnexal appendages
-ectodermal differentiation of totipotential germ cells
-u/l, m/c right
-sebaceous secretion with hair, teeth, bone, cartilage, etc
-prone to torsion
2) Immature malignant -found early
teratomas -bulky, solid on transaction, random necrosis
-differentiation toward cartilage, bone, muscle, nerve, etc
3) Specialized teratomas -struma ovarii – mature thyroid tissues  hyperthyroidism
-small, solid, u/l, brown ovarian masses
-ovarian carcinoid
Disease of Pregnancy
Placental inflmn and -either ascending through birth canal or transplacental
infxn (hematogenous)
-ascending m/c, bacterial, premature birth
 -Candida or mycoplasmas
-hematogenous – syphilis, TB, listeriosis, some viruses
-TORCH complex
Ectopic pregnancy -usually oviducts
Gestational -hydatidiform mole, invasive mole, chroriocarcinoma
Trophoblastic Disease -high hcG
1) hydatidiform mole -like grapes, cystically dilated, chorionic villi
-complete – do NOT have fetal parts, partial does
-abN fertilization
-complete – empty egg with 2 sperm
-partial – normal egg with 2 sperm  triploid
-high hcG with no heart sounds
2) Invasive mole -usually can’t completely remove because invasive
-remain high hcG
3) choriocarcinoma -very aggressive
-from gestational chorionic epithelium or gonads
-bloody, brownish d/c with high hcG w/o uterine enlargement
-usually widespread dissemination
-if from gestational chorionic epithelium 100% cure
Preeclampsia/eclampsia -HTN with proteinuria and edema in 3rd trimester
-eclampsia – seizures  DIC
-inadequate blood to placenta
-usually 24-25 wks

Male Genital System

Penis
Malformations -hypospadias: urethra open on ventral aspect
-epispadias: urethra open on dorsal aspect
-see UTI infections
Inflammatory lesions -often uncircumcised males
1) balanitis and -local inflammation of glans penis or glans and prepuce
balanoposthitis -smegma: desquamated epithelium, sweat, debris
2) phimosis and -prepuce can’t be retracted over glans
paraphimosis -para: stenotic prepuce forcibly retracted
-circulation compromised with resultant congestion
3) genital candidiasis -DM risk
Penile neoplasms -usually squamous cell carcinoma
-usually uncircumcised
-poor hygiene, HPV 16 and 18
-gray, crusted, popular lesion, on glans or prepuce
-uncommon metastases
Scrotum, Testes, -scrotal skin – fungal infections
Epididymis -neoplasms unusual – scc m/c
Hydrocele -m/c cause of scrotal enlargement
-accumulation of serous fluid w/ tunica vaginalis
-infection, tumours, or idiopathic
Hematoceles and -blood or lymph in tunica vaginalis
chyloceles -severe lymphatic obstruction  elephantiasis
Cryptorchidism -failure of testicular descent into scrotum
-malpositioning, hormonal, testicular AbN, mechanical
-b/l  sterility, 4x testicular malignancy
-orchiopexy
Inflammatory lesions -m/c in epididymis
-venereal ds
-nonspecific epididymitis and orchitis: begin as UTI
-orchitis complication of mumps
-TB: epididymitis, 2 to testes, inflammation, necrosis
Testicular neoplasms -m/c cz of firm, painless enlargement of testis
-usu from germ cells (malignant)
-non germ cell may make steroid hormones
-testicular dysgenesis – increase testicular CA
-germ cell tumours 2 categories:
-1) seminomas – single histologic pattern
-2) nonseminomatous germ cell – multiple pattern
-embyonal carcinomas, yolk sac tumours,
choriocarcinomas, teratomas
-tumour markers – hcG and a-fetoprotein
Prostate
Prostatitis -acute bacterial – E.coli, concomitant in urethra and UB
-chronic – bacterial or not (prostatodynia)
Nodular hyperplasia -normal prostate has glandular and stromal elements surrounding
urethra
-aka BPH
-causes: androgens and estrogens
-if castrated before puberty – no incidence
-DHT – stimulate glandular and stromal proliferation
Carcinoma -older males
-androgens play a part
-if castrated, no development
-bone mets are common
-PSA – early dx
STD
Syphilis -T pallidum
-human only natural hosts
-active cutaneous or mucosal lesion
-can be congenital
-common in HIV px
Primary syphilis -hard chancre
-painless, well-defined indurated margins, moist base
-see spirochetes
-serologic tests often negative in early stages
-self limiting
Secondary syphilis -w/in 2 months of primary
-palms, soles, feet
-condylomata lata – broad, elevated, moist areas
-last several weeks, then 1 year latent phase
-strongly positive Ab tests
Tertiary syphilis -1/3 px after 5 years
-nontreponemal Ab may be –ve, antitreponemal Ab +ve
Congenital syphilis -can lead to stillbirth
-infantile – chronic rhinitis, desquamating rash
-late or tardive – Hutchinson triad: notched central incisors,
interstitial keratitis with blindness, deafness from CN VIII
-saddle nose, mulberry molars
Serological tests for -non-treponemal Ab and antitreponemal Ab tests
Syphilis -non-treponemal Ab – often –ve in early stages of disease
-antitreponemal Ab tests – T. pallidum Antibodies
Gonorrhea -humans only natural host
-need direct contact with mucosa
-in females – lead to salpingitis, infertility
-disseminated infection: less common
-sxs: tenosynovitis, arthritis, skin lesions
-rare endocarditis and meningitis
-gonococcal infection – can go to infants – opthalmia neonatorum
Nongonococcal Urethritis -m/c STD today
and Cervicitis -C trachomatis, t. vaginalis, u. urealyticm, m. hominis
-C trachomatis: gram –ve, indistinguishable from N. gonorrhoeae
-HLA-B27 +ve
-Reiter’s syndrome
Lymphogranuloma -chronic, ulcerative ds
Venereum -C. trachomatis
-sexual promiscuity
Chancroid (soft chancre) -acute, ulcerative
-H ducreyi
-lower SES, tropical areas
-m/c cause of genital ulcers in Africa and SE Asia
-co-factor for HIV-1
Granuloma Inguinale -chronic inflmn
-c. donovani
-rural and tropical areas
-sexual promiscuity
-scarring, elephantiasis
Trichomoniasis -t vaginalis
-sticks to mucosa
-itchy, profuse, frothy, yellow vaginal d/c
-dysuria
-often asxs in males – but can look like nongonococcal urethritis
Genital Herpes Simplex -HSV 2
-direct contact with mucosal surface
-neonatal herpes infection
HPV -codylomata acuminate – venereal warts – HPV 6 and 11
-cervical CA – HPV 16 (also 18, 31, 45)

KI and Collecting System

Manifestations of Renal -azotemia – elevation of blood urea nitrogen and creatinine
Diseases -related to decrease GFR
 -uremia – when azotemia has clinical ss/sxs and biochem abN
Glomerular Disease -glomerular capillary wall has fenestrated endothelial cells, GBM,
visceral epithelial cells (podocytes) and foot processes (pedicels)
-supported by mesangial cells (contractile and secretes
-GFR: high permeable to water and small solutes)
-secondary glomerular diseases: affect glomerulus
-primary GN or glomerulopathy – affect KI
-2 forms of Ab-associated injury:
-1) deposits of circulating Ag-Ab complexes in glomerulus
-glomerulus does not incite rxn
-Ag endogenous or exogenous
-if Ag exposure cts, repeated immune cycles chronic
-2) Ab reacting in situ in glomerulus
Immune Complex -anti-glomerular basement membrane disease
Nephritis in Situ -Ab vs fixed Ag in GBM
-spontaneous anti-GBM nephritis – autoAb vs GBM
-Goodpasture syndrome – anti-GBM cross-react in LU and KI
-severe glomerular damage
Cell Mediated Immune -sensitized T cells from cell-mediated immune rxn
GN
Mediators of Immune -glomeular damage, loss of barrier function
injury -proteinuria and mb reduced GFR
-complement-leukocyte-mediated mechanism – mainly C5a and
recruit neutrophiles and monocytes
-neutorphils release proteases  destroy GMB
-free radicals  Cell damage
-arachidonic acid  reduce GFR
Epithelial Cell Injury -Abs to epithelial cell Ag or toxin
-see morphologic change in visceral epithelial cells
-proteinuria
-detachment of visceral epithelial cells caused by alterations in
nephrin and cytoskeletal proteins
-protein leakage
Renal Ablation -reduce GFR to 30-50%  end stage renal ds
glomerulopathy -proteinuria and glomerulosclerosis
-rest of glomeruli hypertrophy  handle additional load  injury
 capillary collapse and sclerosis
Nephrotic Syndrome -1) massive proteinuria
-2) hypoalbuminemia
-3) edema
-4) hyperlipidemia and lipiduria
-increase permeability to plasma proteins
-depleted serum albumin
-edema d/t decrease osmotic P b/c hypoalbuminemia and primary
retention of salt and water by KI  decrease plasma volume 
decrease GFR  aldosterone secretion promotes retention of salt
and water
-adults usu systemic ds; children usu KI prob
-systemic: DM, amyloidosis, SLE

1) minimal change disease
2) Membranous GN
3) focal glomerulosclerosis
4)membranoproliferative
GN
Nephritic Syndrome
Acute Prolif GN
Berger Disease
-primary glomerular lesions: membranous GN, lipid nephrosis
(minimal change disease), focal glomerulosclerosis,
membranoprolif GN
-benign ds, m/c caouse of nephrotic syndrome in children
-glomeruli that look normal in light microscope but diffuse loss of
epithelial foot processes in electron microsope
-ds of T cells  loss foot processes and proteinuria
-subepithelial Ig deposits in GBM
-diffuse thickening of capillary wall
-cz: infections, tumours, SLE, AI conditions, inorganic salts,
NSAIDs, idiopathic
-Abs react to endogenous glomerular Ag
-Heymann nephritis – idiopathic MGN
-C5b-C9 on cell  leaky and liberates proteases and oxidants
-sclerosis affecting some but not all glomeruli and only segments of
each glomerulus
-IgM
-injury  disrupts epithelial cells
-mb ass with nephrotic syndrome
-can occur with HIV, heroin, secondary, congenitally, primary, or
part of glomerular ablation nephropathy
-hematuria and HTN
-proteinura  renal ds
-no response to corticosteroids
-altered BM and mesangium, prolif of glomerular cells
-2 types
-1) immune complexes with hep B and C, SLE, infxn
-2) C3 nephritic factor  alt complement pathway
-hypocomplementemia (more type II)
-acute onset
-1) hematuria
-2) oliguria and azotemia
-3) HTN
-some proteinuria and edema
-maybe SLE or primary glomerular ds
-post strep, postinfectious
-1-4 weeks in child after group A strep
-usu initial infxn in pharynx or skin
-immune complex with IgG and complement on GBM
-hypocomplementemia
-IgA nephropathy
-children and young adults
-1-2 days after URTI
-gross hematuria, every couple months, loin pain
-IgA in mesangium
-over IgA production
-celiac ds
-LV ds – defective hepatobiliary clearance of IgA (secondary IgA
nephropathy)
-m/c of glomerular disease
Hereditary Nephritis
Chronic GN
Ds affecting Tubules and
Interstitium
Tubulointerstitial Nephritis
1) acute pyelonephritis
2) chronic pyelonephritis
Drug induced interstitial
nephritis
Acute Tubular Necrosis
Ds involving BV
Benign Nephrosclerosis
Malignant HTN and
nephrosclerosis
Thrombotic
microangiopathies
-Alport syndrome – nephritis with deafness, eye ds
-BM defect
-chromo 2
-cause end stage renal ds
-develops insidiously
-tubular injury
-bacterial
-renal pelvis
-pyelonephritis
-interstitial nephritis – noninfxs
-acute or chronic
-UTI
-E. coli, proteus, klebsiella, enterobacter, pseudomonas
-recurrent infections
-either by bloodstream of LUTI, more in females
-interstitial inflammation and scarring in renal parenchyma
-deformity of pelvicalyceal system
-cause of chronic renal failure:
-1) chronic obstructive PN
-2) reflux PN – superimposed UTI on veicoureteral reflux and
intrarenal reflux  chronic renal insufficiency
-1) acute – m/c synthetic penicillin, 15 days post exposure
-sxs: fever, eosinophilia, rash, renal abN
-drugs act as haptens, bind to tubular  immunogenic
-IgE
-2) analgesic – large consumption  chronic inflmn often with
renal papillary necrosis
-mix drus
-covalent damage and oxidative damage
-inhibit PG synthesis  ischemia (loss of v-dilation)
-destruction of tubular epithelial cells and acute suppression of renal
function
-m/c cause of acute renatl failure
-24 hr urine < 400mL
-d/t inadequate blood flow, or nephrotoxic
-benign HTN with hyaline arteriolosclerosis
-usu with primary KI dx
-mild proteinuria
-usu die of HTN HT ds or CV prob
-less common
-renal vascular damage (d/t benign one or arteritis or sclerotic
injury)  renal ischemia  stim angiotensin sys  v-constriction
 more ischemia
-malignant arteriolosclerosis – HT throughout body
-microangiopathic hemolytic anemia, thrombocytopenia, renal
failure
-childhood HUS – follow E.coli
 -major cause of acute renal failure in children
-bacterial verocytotoxin on endo  thrombosis, v-constrict
Cystic Dx of KI
Simple Cysts -innocuous
-fill with clear fluid
-usu in cortex
-dialysis-associated acquired cysts – end stage renal ds with prolong
dialysis, in cortex and medulla, hematuria
Polycystic KI ds -adult
-autosomal dominant
-chromo 4 or 16
-multiple expanding cysts in both KI, destroy parenchyma
-child
-autosomal recessive
-chromo 6
-small cysts in cortex and medulla
Urinary Outflow Obs
Renal stones -urolithiasis
-predispose to bacterial infxn
-increased urine concentration, supersaturation
-most likely calcium, hypercalciuri/emia
-Mg ammonium P (struvite) – UTI
-uric acid stones – gout and leukemias
-cystine stones – defect in renal transport
Hydronephrosis -dilation of renal pelvis and calyces
-atrophy of parenchyma b/c obs of urine flow
-congenital or acquired
-below ureters – b/l; above or at – u/l
-still have glomerular filtration  affected calyces and pelvis
become dilated
Tumours -LUT are 2x as common as renal cell carcinomas
Renal Cell Carcinoma -cortical
-LT dialysis, smoking, cadmium
-1) clear cell carcinoma
-2) papillary renal cell carcinoma: MET protooncogene
-3) chromophobe renal carcinoma – good prog
Wilms Tumour -more common in young children
-all mesodermal
Tumours in UB and -transitional epithelium  epithelial tumours
collecting system -UB common  50x more if exposed to b-naphthylamine
-can recur and infiltrative obs of ureters rather than malignant

MSK System
Hereditary Diseases of
Bone
Achondroplasia -inherited
-impaired maturation of cartilage
-cause dwarfism – osteochondrodysplasia
-constant activate fibroblast growth factor receptor 3 on chromo 4
(supposed to inhibit normal cartilage prolif)
-shortening of proximal extremities, bowing legs, lordotic
Osteogenesis imperfecta -“brittle bone ds”
-abN development of type I collagen (sin, joints, eyes)
-varying severity of bone fragility
-multiple bone fractures
-can result in abN dentition, hearing loss, blue sclera
Osteopetrosis -“marble bone ds”
-deficient osteoclastic activity
-abnormally thickened, mineralized brittle bone
-anemia, thrombocytopenia, infections, fractures
-dramatic decrease amt of marrow space for hematopoiesis
-can compress nerve roots  CN palsies
Osteoporosis and
acquired metabolic ds
Osteoporosis -low bone mass, deterioration with increase in bone fragility and
susceptibility to fractures
-senile osteop
-postmenopausal osteo – women after menopause
-bone resorption > formation
-RANK ligand has to be expressed on stromal cells or osteoblasts so
macrophages can differentiate into osteoclasts
-RANK R is stimulus to bone resorption
-peak bone mass important determinant of risk
-most vulnerable white females
-spine and femoral necks – common fracture site
-decrease in osteoblastic and increase in osteoclastic activity
-hormonal factors, need estrogen
-genetic factors: need Vit D
-mechanical – weight bearing
-diet – Ca and vit D
Rickets and Osteomalacia -vit D xu - defective mineralization of bone
-increase nonmineralized osteoid
-osteo – total bone decrease but mineral content of remaining bone
is normal
-rickets – children
-osteomalacia – defective mineralization of bone that has completed
its normal development
Bone Ds Associated with -PTH – calcium homeostasis (osteoclast activation, increased bone
Hyperparathyroidism resorption, calcium mobilization, increase resoprtion of Ca by renal
tubules, increase vit D by KI which increases Ca absorption from
gut and moves Ca from bone)
-net effect: raise serum Ca level, should inhibit further PTH
-xs PTH, renal insufficiency (no vit D)  abN osteoclasts
Osteomyelitis -Inflammation of bone and marrow cavity
-infections only
Pyogenic Osteomyelitis -3 routes: hematogenous, direct extension nearby, surgical
-Staph aureus – m/c  has R for bone matrix that help stick
-chronic is sequelae
-sequestrum (necrotic bone), if big, surrounded by rim of reactive
bone called involucrum
-Brodie abscess – rim with residual abscess
-organisms can live in sequestered area
Tuberculous Osteomyelitis -hematogenous spread
-long bones and vertebrae
-synovium common site of initial infection  epiphysis 
inflammatory rxn with necrosis and bone destruction
-Pott disease  TB of vertebral bodies
-cold abscess in psoas
Paget Disease -aka Osteitis Deformans
-osteoclastic  mixed clast and blast  osteosclerotic phase
(dense, mineralized bone with little cellular activity)
-end result: xs abN, unstable bone
-infection? Paramyxovirus-like
Bone Tumours -more metastatic lesions – prostate, breat, LU, KI, GIT, thy
-usu osteolytic (prostate  blast)
Bone forming tumours -production of osteoid by neoplastic cells
-osteoblastic metastases – osteoid by osteoblasts
1) osteoma -reactive growth
-head and neck
-localized, solitary hard growth on surface of bone
-Gardner syndrome – multiple lesions
-not malignant
2) osteoid osteoma and -benign neoplasms
osteoblastoma -osteoid osteoma: femur, tibia, males, <2cm,local pain relieved by
aspirin
-osteoblastomas: vertebral column, males, pain, hard to localize, not
responsive to ASA
3) osteosarcoma -malignant
(Terry Fox) -neoplastic cells make osteoid
-primary and secondary forms
-knee, distal femur, proximal tibia
-males, TP53 tumour suppressor gene
Cartilaginous Tumours
1) osteochondroma -aka exostoses – benign prolif with bone and cartilaginous cap
-mostly asxs
-from metaphysis  bony firmly anchored with cap of hyaline
cartilage
-stop once skeletal growth completed
2) Chondroma -mature hyaline cargilate
-hands and feet
-Ollier ds – multiple, one side of body
-Maffucci syndrome – multiple chondroma with angiomas
-well-circumscribed lesion in medullary cavity of bone
-multiple ones  chondrosarcomas
3) Chondrosarcoma -malignant neoplasms with mesenchymal cells that make
cartilaginous matrix
-neoplatic cells do NOT form osteoid
Other Tumour Stuff
Giant Cell Tumour -aka osteoclastoma
-epiphyses
-giant cells with mononuclear cells
Ewing Sarcoma Family -EWS and PNET
-neural origin and presence of chromosomal translocations
Fibrous Dysplasia -normal trabecular bone replaced by fibrous tissues and malformed
bone
-m/c monostotic fibrous dysplasia – from teens
-polyostotic fibrous
-polyostotic fibrous with endocrime – café au lait, precocious
puberty (McCune-Albright syndrome)
Diseases of Joints
1) OA -aka degenerative joint disease
-degeneration of articular cartilage
-not really inflammation
-aging and mechanical effects
-Herberden nodes
2) Gout -tissue accumulation of xs uric acid (purine met)
-tophi – large crystalline aggregates
-primary overproduction of uric acid
-Lyesch-Nyhan syndrome – last HGPRT, only males (x-linked), xs
uric acid, severe neurological ds, self mutilation
3) infectious arthritis -salmonella if px has sickle cell
-with local pain, fever, neutrophilic inflmn
-Lyme Ds – Borrelia burgdorferi, deer ticks
-3 stages: erythema chronicum migrans, early disseminated stage,
late disseminated stage
-chornic arthritis, smtms with severe damage to large joint and
encephalitis
Ds of Skeletal Muscle
Neurogenic Atrophy -ex: floppy infant syndrome
-progressive atrophy
Type II Myofiber atrophy -bedridden with glucocorticoid usage
-endogenous hypercortisolism
-type II – fast twitch
Myasthenia Gravis -acquired AI
-Ab vs Ach-R
Lambert-Eaton -usually with small cell carcinoma of LU
Myasthenic Syndrome -increase in amp of AP with repetitive stimulation
-Ab vs presynp of NMJ
Inflammatory Myopathies -polymyositis and dermatomyositis
-idiopathic, m/b parasites or viral
Muscular Dystrophies -spontaneous, progressive degeneration of MSK fibers
Duchenne and Becker -DMD – X-lined, absence of dystrophin
Muscular Dystrophy -impaired conractile activity
-BMD – x linked, mutation of dystrophin gene
 -Less severe that DMD
Other Myopathies -intrinsic metabolic errors and exogenous toxic insult
Soft Tissue Tumours -usu benign
-local mass
Tumours of Adipose -lipoma – subQ tissue, sporadic lesions, slowly enlarging
-liposarcoma – malignant neoplasms of adipocytes, visceral sites,
lower extremity, and abdomen, often to LU
Tumour-Like lesions of
fibrous tissue
Nodular fasciitis -self-limited, reactive fibroblastic
-rapidly enlarging, may be painful
-usually upper extremity and trunk, hx of local trauma
Fibromatoses -grow in infiltrative fashion
-superficial – dupuytren contracture, penile fibromatosis (Peyronie
ds) – structural deformity
-deep – abdomen, trunk, extremeties
-can be part of Gardner syndrome – polyps in colon, osteomas of
bone, fibromatsoses
Fibrosarcoma -malignant neoplasms of fibroblasts
-keep tissues in thigh, knee, and retroperitoneal area
-slow growth, recur often to LU
Fibrohystiocytic tumours
a) fibrous histiocytoma -well-defined mobile nodule in dermis or subQ
-interlacing spindle cells
b) dermatofibrosarcoma -intermediate tumour b/w benign and malignant
protuberans -dermis and subQ, slow growing
-often recur, infiltrative
c) malignant fibrous -aggressive soft tissue sarcoma, aggressive
histiocytoma -deep muscular tissues in extremities, retroperitoneal area
Neoplasms of MSK
Rhabdomyosacoma -neoplasm of infancy, childhood, and teens
-malignant mesenchymal neoplasm
-embryonal rhabdomyosarcoma
-in head, neck, GUT, retroperitoneum
-alveolar rhabdomyosarcoma – extremity
-pleomorphic rhabdomyosarcoma – rare in soft tissue
Smooth Muscle Tumour -leiomyomas - benign
-leiomyosarcoma – malignant smooth muscle tumours
Misc Neoplasms -synovial sarcoma – mesenchymal cells around joints (not always),
chromosomal translocation